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Abstract Functional recovery after spinal cord injury (SCI) remains challenging, requiring therapeutic targets. Here, we show that doublecortin-like kinase 1 (DCLK1) is upregulated after SCI in mice. Pharmacological inhibition of DCLK1 with DCLK1-IN-1 improved motor recovery, reduced glial scar formation and fibrosis, and preserved neurons at the lesion site. Mechanistically, we identified the microtubule-severing protein KATNA1 as a downstream target of DCLK1.
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